Interleukin-22 Influences the Th1/Th17 Axis

Abstract

Interleukin-22 (IL-22) is secreted by a wide range of immune cells and its downstream effects are mediated by the IL-22 receptor, which is present on non-immune cells in many organs throughout the body. IL-22 is an inflammatory mediator that conditions the tissue compartment by upregulating innate immune responses and is also a homeostatic factor that promotes tissue integrity and regeneration. Interestingly, the IL-22 system has also been linked to many T cell driven inflammatory diseases. Despite this, the downstream effects of IL-22 on the adaptive immune system has received little attention. We have reviewed the literature for experimental data that suggest IL-22 mediated effects on T cells, either transduced directly or via mediators expressed by innate immune cells or non-immune cells in response to IL-22. Collectively, the reviewed data indicate that IL-22 has a hitherto unappreciated influence on T helper cell polarization, or the secretion of signature cytokines, that is context dependent but in many cases results in a reduction of the Th1 type response and to some extent promotion of regulatory T cells. Further studies are needed that specifically address these aspects of IL-22 signaling, which can benefit the understanding and treatment of a wide range of diseases.

Probiotics to manage inflammation in HIV infection

“…IL-22 is a member of the IL-10 cytokine family, and are produced by Th22 cells, Th17 cells, Th1 cells, ILC3, some CD8+ T cells, γδ T cells and other cell types in response to different stimuli (135,136). Naïve CD4+ T cells differentiate into Th22 cells in the presence of IL-6 and tumor necrosis factor (TNF)a (133).…”

Types of necroinflammation, the effect of cell death modalities on sterile inflammation

“…Some human ILC3 cells co-express CD39 and CD73, especially after IL-1β stimulation. In addition, the extracellular ATP-activated ILC3 cells produce IL-22, a typical cytokine of the Th17 response [ 78 ]. Additionally, increased amounts of ILC3 cells are associated with upregulated levels of IL-1β and aggravates inflammatory arthritis in mice lacking phagocytic NADPH oxidase.…”

Vitamin D, Th17 Lymphocytes, and Breast Cancer

“…Moreover, Th17/Th1 cells produce both IL-17 and IFNγ and Th17 cells stimulated by IL-12 can shift to Th17/Th1 [ 205 , 206 ]. Activated Th17 cells can produce IL-22 along with IL-17 [ 207 ], and represent a distinct population apart from Th22 cells [ 208 ]. Intestinal Th17 cells can differentiate into T follicular helper (Tfh) cells in Peyer’s patches [ 209 ].…”